Fig. 1: Mice deficient in p63γ have a short lifespan and are prone to spontaneous tumors.
From: TAp63γ is the primary isoform of TP63 for tumor suppression but not development
A The TP63 gene locus, the P1 promoter for TAp63, and the P2 promoter for ΔNp63. B The structure and functional domains of TAp63α, ΔNp63, and TAp63γ proteins. AD: activation domain. PRD: proline-rich domain. DBD: DNA-binding domain. TD: tetramerization domain. SAM: sterile alpha motif. C The strategy to knock out p63γ-specific exon 10’. The location and sequence of the two sgRNAs and the location of p63γ-F/R primers are indicated. The predicted double-strand breaks near the PAM motifs (in red) are indicated by double blue arrow. Founder #18 has a deletion of 161 nucleotides spanning from intron 10 to exon 10’, including the splice acceptor site (AG). D Genotyping of wild-type and p63g-null alleles of Wild-type, p63γ+/−, and p63γ−/− MEFs. E Kaplan–Meier survival curves of WT (n = 56), TAp63+/− (n = 21), p63γ+/− (n = 20), and p63γ−/− (n = 33) mice. F Representative images of H.E.-stained lung adenocarcinoma in p63γ-null mouse #74 and hepatocellular carcinoma in p63γ-null mouse #128.
